The umbilical vessels have thick muscular walls that react to trauma, tension, sympathomimetic amines, bradykinin, angiotensin, and changes in PO2. In animals in which the umbilical cord is not tied, hemorrhage of the newborn is minimized by constriction of these large umbilical vessels in response to stretching of the umbilical arteries and by an associated increase in PO2 in systemic arteries.
Closure of the umbilical vessels increases total peripheral resistance and the arterial blood pressure of the infant. When blood flow through the umbilical vein ceases, the ductus venosus, a thick-walled vessel with a muscular sphincter, closes. The factor that initiates closure of the ductus venosus is unknown.
Ifapregnantwomanissubjectedtohypoxia,thereducedbloodPO2inthefetusevokestachycardiaandanincreaseinbloodflowthroughtheumbilicalvessels.Ifthehypoxiapersistsorifflowthroughtheumbilicalvesselsisimpaired,fetaldistressoccursandismanifestedinitiallyasbradycardia.
•Fig. 17.44 Schematic Diagram of the Fetal Circulation. Thenumbers representthepercentageofO2saturationofthebloodflowingintheindicatedbloodvessel.Fetalbloodthatleavestheplacentais80%saturated,butthesaturationofthebloodthatpassesthroughtheforamenovaleisreducedto67%.ThisreductioninO2saturationiscausedbythemixingofsaturatedbloodwithdesaturatedbloodreturningfromthelowerpartofthefetalbodyandtheliver.AdditionofthedesaturatedbloodfromthefetallungsreducestheO2saturationofleftventricularbloodto62%,whichisthelevelofsaturationofthebloodreachingthefetalheadandupperextremities.Thebloodintherightventricle—whichisamixtureofdesaturatedsuperiorvenacavalblood,coronaryvenousblood,andinferiorvenacavalblood—isonly52%saturatedwithO2.Whenthemajorportionofthisbloodtraversestheductusarteriosusandjoinsthatpumpedbytheleftventricle,theresultingO2saturationofthebloodtravelingtothelowerpartofthefetalbodyandbacktotheplacentais58%.Theinset atupperleftillustratesthedirectionofflowofamajorportionoftheinferiorvenacavalbloodthroughtheforamenovaletotheleftatrium.Arrows indicatethedirectionsofflow.(DatafromDawesGS,etal.J Physiol. 1954;126:563.)
Immediately after birth, the asphyxia caused by constriction or clamping of the umbilical vessels, together with cooling of the body, activates the respiratory center of the newborn infant. As the lungs fill with air, pulmonary vascular resistance decreases to approximately 10% of the value that existed before lung expansion. This change in vascular resistance is not caused by the presence of O2 in the lungs because the change is just as great if the lungs are filled with N2. However, filling the lungs with liquid does not reduce pulmonary vascular resistance.
After birth, left atrial pressure is raised above that in the inferior vena cava and right atrium by (1) the decrease in pulmonary resistance, with the consequent large flow of blood through the lungs to the left atrium; (2) the reduction of flow to the right atrium caused by occlusion of the umbilical vein; and (3) the increased resistance to left ventricular output produced by occlusion of the umbilical arteries. Reversal of the pressure gradient across the atria abruptly closes the valve over the foramen ovale, and the septal leaflets fuse over a period of several days.